Chapter 41 Cyanobacteria
SOURCES
Blue-green algae (cyanobacteria) are commonly found growing in fresh and salt water in temperate areas worldwide. In the United States, they often are found in freshwater ponds, lakes, rivers, streams, canals, and ditches. Under appropriate climatic and nutritional conditions, very rapid growth of blue-green algae results in “blooms” that rise and accumulate at the surface of the water and sometimes produce hepatotoxins and/or neurotoxins. A single bloom can consist of more than one type of cyanobacteria. Blooms of blue-green algae in the northern United States often occur from late summer to early winter (although they can occur anytime throughout the year) and are commonly associated with periods of hot, calm weather, decreased rainfall, increased nutrients (e.g., nitrate, phosphate, sulphate) in the water, and with winds that blow and concentrate the algae along the shore. Blooms can occur all year long in southern states when all the environmental and nutritional conditions are met.
TOXIC DOSE
The blue-green algae Microcystis and Nodularia can produce the cyclic peptide hepatotoxins microcystin and nodularin, and Anabaena, Aphanizomenon, Lyngbya, and Oscillatoria can produce the neurotoxins anatoxin-a and anatoxin-a(s). It has been difficult to calculate what a “toxic-lethal” dose is for dogs and cats; the number of cyanobacteria and concentrations of toxins vary considerably among blooms. However, based on case reports, toxicities and lethalities have been observed in dogs following single exposures to contaminated water through drinking or consuming water while swimming.
MECHANISM OF TOXICITY
Toxicoses have been reported in dogs following ingestion of water containing blue-green algae. Cats appear to be less commonly affected, even though all species are considered to be susceptible to the effects of the toxins. Not all blue-green algae blooms produce toxins, and the specific water conditions that support toxin development have not been firmly established. The hepatotoxins microcystin and nodularin are rapidly absorbed from the intestine following ingestion and are subsequently taken up by hepatocytes via a specific carrier-mediated uptake mechanism. There they inhibit protein phosphatases, which initiate a cascade of events leading to a rapid, massive hepatocyte necrosis, intrahepatic hemorrhage, and shock.
The neurotoxin anatoxin-a is a potent postsynaptic depolarizing neuromuscular blocking agent, whereas anatoxin-a(s) is a potent acetylcholinesterase inhibitor. Both compounds are rapidly absorbed from the small intestine following ingestion.
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